EMBL Researchers Create the First Models of Parasitic Gliding Functions

Researchers from The European Molecular Biology Laboratory (EMBL) have been studying the unique gliding behavior of parasites that cause malaria and toxoplasmosis, a disease caused by the Toxoplasma gondii parasite. The study was recently published in the Nature journal Communications Biology.

Gliding motility refers to the unique movement of apicomplexan parasites who can cross biological barriers without changing their form. Their movement is powered by a group of proteins called the glideosome.

Actins are proteins that form microfilaments and are found in all eukaryotic cells. Myosins are motor proteins that are responsible for muscle contraction and motility for all vertebrates and eukaryotes.

Gliding Parasites

Apicomplexan parasites cause thousands of deaths per year through infections and malaria. The parasites are also pests to the agricultural industry.

Malaria, caused by the Plasmodium species, causes nearly 414,000 deaths every year and more than 220 million infections. The parasite Toxoplasma gondii infects up to 30% of people around the world, who show no clinical symptoms. However, the parasite causes severe damage to pregnant women and those who are immunocompromised.

Both parasites are transmitted through mosquitoes and cats. When a person gets an infected mosquito bite, Plasmodium glides through the skin and enters the bloodstream.

The glideosome is the interaction between myosin and other proteins within apicomplexan parasites. Very little is known about the molecular structure of glideosome proteins. Understanding the protein structures could advance the development of drugs to prevent glideosome proteins from the assembly. New treatment could then be developed for malaria and toxoplasmosis.

Molecular Structure of Parasite Proteins

The team was able to create the molecular structure of glideosome proteins called essential light chains (ELC) which bind to the parasite's myosin. They used a combination of nuclear magnetic resonance and X-ray crystallography.

They observed that after the ELCs bound with the myosin, they became rigid and functioned as the parasite's lever arm. The proteins enabled the parasite to take long steps and accelerate gliding motility. The researchers also discovered that calcium does not influence the protein structure from becoming stiff but helps stabilize the ELCs.

Matthew Bowler, who studies Toxoplasma parasites in the immune system but was not involved in the study said that the paper is an initial glimpse of how the two parasites move around and cause infection. "It is fascinating to see new molecular details emerge on how these parasites work outside of the host cell. The beautiful structures show how the motor that drives this motion is put together and could provide a basis to develop new medicines to treat these diseases."

Maria Bernabau, also not involved in the research but leads research on cerebral malaria, said, that infection caused by Plasmodium begins as it glides through the skin. "Understanding the parasite's gliding motility might help to develop drugs or vaccines that target Plasmodium before it multiplies."

In conclusion, the authors wrote that ELCs can double the speed of myosin within the parasites. Further studies are needed to fully understand the glideosome structure and mechanism of apicomplexan gliding.

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